Phencyclidine (PCP) Toxicity


Article Author:
Jonathan Journey


Article Editor:
Thomas Bentley


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
6/4/2019 7:51:04 PM

Introduction

Phencyclidine (PCP) is a dissociative anesthetic that is a commonly used recreational drug. PCP is a crystalline powder that can be ingested orally, injected intravenously, inhaled, or smoked. After being discovered in 1926, PCP was developed as a general anesthetic in the 1950s because it could achieve analgesia and anesthesia with minimal cardiovascular and respiratory suppression. It was marketed under the name Sernyl. In 1963, Sernyl began to be used in surgical procedures. By 1967, it was discontinued due to postoperative dysphoria and hallucinations. After 1967, it was limited to veterinary use. Also in the 1960s, PCP began to be illegally manufactured in laboratories and emerged as a popular street drug in San Francisco. In the 1970s, PCP use became widespread. Common street names for PCP are the peace pill, angel dust, crystal joints, rocket fuel, sawgrass, zoom, the sheets and elephant tranquilizer. Depending on the dose and route of administration, PCP can have a wide range of central nervous system (CNS) manifestations. Emergency department providers should become familiar with how to manage patients with PCP toxicity since rhabdomyolysis, hypoglycemia, seizures, hypertensive crisis, coma, and trauma are several of the complications that can arise with PCP use[1].

Etiology

PCP toxicity is caused by use and abuse of phencyclidine.[2][3][4]

Epidemiology

There were 75,538 emergency department visits in 2011 due to PCP, according to the Drug Abuse Warning Network. This was up 400% from 2005 (14,825). Seventy-two percent of PCP-related emergency department visits in 2011 involved PCP used in combination with other drugs such as marijuana, cocaine, analgesics, and anxiolytics. The majority of emergency department visits due to PCP in 2011 involved male patients (69%). Forty-five percent were patients who were 25 to 34 years old. Patients who were aged 18 to 24 years old and 35 to 44 years old accounted for 19% of emergency department visits each. According to the American Association of Poison Control Centers, there were two deaths from PCP in 2012.  

Pathophysiology

PCP is available as a powder, crystal, liquid, and tablet. It produces both stimulation and depression of the CNS. PCP is a noncompetitive antagonist to the NMDA receptor, which causes analgesia, anesthesia, cognitive defects, and psychosis. PCP blocks the uptake of dopamine and norepinephrine, leading to sympathomimetic effects such as hypertension, tachycardia, bronchodilation, and agitation. PCP can also cause sedation, muscarinic, and nicotinic signs by binding to acetylcholine receptors and GABA receptors. Sigma receptor stimulation by PCP causes lethargy and coma.[5][6][7]

Toxicokinetics

PCP, also known as 1-(1-phenylcyclohexyl-piperidine), is a synthetic arycycloalkylamine created from piperidine and cyclohexanone. It has a volume distribution of 6.2 L/kg and a pH between 8.6 and 9.4. It is soluble in water and ethanol. PCP begins to cause symptoms at a dose of 0.05mg/kg, and a dose of 20 mg or more can cause seizures, coma, and death. It is mainly metabolized by the liver, and 10% is excreted in the kidneys. Inhalation (the most common route of administration) and intravenous routes of administration produce symptoms in 2 to 5 minutes. Oral ingestion produces symptoms in 30 to 60 minutes. The half-life is estimated to be 21 hours, but symptoms can last from several hours up to 48 hours, depending on the dose. Recurrent, fluctuating symptoms can occur because PCP is fat-soluble and can be released from lipid stores and adipose tissue that can occur days to months after the initial use.

History and Physical

Depending on the dose, administration route, and coingestants, PCP can cause a wide spectrum of clinical effects, from coma to extreme agitation or psychosis. Many times, patients are unable to give a clear history, so it is imperative to attempt to obtain a history from emergency medical personnel, family, friends, and witnesses. Familiarity with the street names for PCP can be helpful as well.

  • General - ranging from coma to severe agitation, hyperthermia, hypoxia
  • HEENT– Nystagmus, horizontal, vertical, rotary (60%- 90%), miosis
  • Cardiovascular – hypertension (60%), tachycardia (30%)
  • Neurological – mild to severe agitation, confusion, hallucinations, delusions, violent behavior, seizures, muscle rigidity, ataxia, coma
  • Trauma - thorough examination for evidence of trauma should be completed as injuries secondary to PCP intoxication can occur due to the agitation, hallucinations, diminished perception of pain, and delusions of increased physical ability

Evaluation

The evaluation should include the following:

  • Serum PCP level -  not available at many hospitals
  • Fingerstick blood glucose - present in 22% of cases of PCP toxicity
  • Complete blood count–leukocytosis can be seen
  • Electrolyte panel–BUN and creatinine can be elevated
  • Creatine kinase– elevated it in 70% of cases with PCP toxicity
  • Acetaminophen and salicylate levels–to evaluate for other coingestions
  • Electrocardiogram – to evaluation for conduction abnormalities
  • Consider CT head – to rule out other causes of altered mental status
  • Consider cerebral spinal fluid evaluation – to rule out CNS infection
  • Urine toxicology screen – can be helpful to identify coingestions, but may not be helpful to identify acute PCP intoxication because chronic PCP users can have a positive test weeks after their last use. False positives occur for PCP with methadone, ibuprofen, venlafaxine, and chlorpromazine use
  • Liver function test – elevated in 50% of cases with PCP toxicity
  • Urinalysis -  elevated myoglobin levels
  • Imaging studies-  should be performed when there is a concern for trauma secondary to PCP intoxication

Treatment / Management

Most patients survive PCP intoxication with supportive care. Airway, breathing, circulation, and hemodynamic monitoring are essential to the care of patients with PCP toxicity. Intubation with ventilatory support may be required for airway protection.

Gastrointestinal decontamination is generally unnecessary in PCP ingestions; however, activated charcoal may be beneficial with a massive ingestion of PCP or a dangerous coingestion. Activated charcoal therapy should only be started within one hour from the time of ingestion. The activated charcoal dose is 1 g/kg, with a maximum dose of 50 g.

Sedation with medication and physical restraints may be required to control agitation, violent behavior, and psychosis due to PCP intoxication. Placing the patient in a calm environment such as a quiet room with the lights dimmed may be helpful. Benzodiazepines are the preferred medication for chemical sedation in patients with PCP toxicity. Lorazepam 2 to 4 mg intravenous (IV) or intramuscular (IM), or diazepam 5 to 10 mg IV or IM are recommended. Repeated doses every 10 minutes may be required for adequate sedation. Benzodiazepines are also the first-line treatment for PCP-induced hypertension and seizures. Hyperthermia from PCP toxicity is due to psychomotor agitation and can be successfully treated with benzodiazepines as well.

Patients with mild symptoms can be discharged one to 2 hours after they become symptom-free and have no other medical complications or behavioral issues that need to be addressed. Patients with severe symptoms or medical complications should be admitted to a monitored bed. Patients who are asymptomatic who present to the emergency department after PCP use should be observed for at least 6 hours before being discharged. Psychiatric evaluation should be considered in patients whose medical symptoms/complications have resolved but required further management of behavioral issues.

Differential Diagnosis

  • Alcohol intoxication
  • Amphetamine intoxication
  • Anticholinergic poisoning
  • Bipolar disorder
  • Brain neoplasms
  • Cocaine toxicity
  • Diphenhydramine toxicity
  • Delirium tremors
  • Encephalitis
  • Hyperthyroidism
  • Hypoglycemia
  • Hyponatremia
  • Hypoxia
  • Lysergic acid diethylamide (LSD) toxicity
  • Malignant hyperthermia
  • MDMA toxicity
  • Neuroleptic malignant syndrome
  • Serotonin syndrome
  • Salicylate poisoning
  • Toxic alcohol poisoning
  • Trauma  (self-induced or accidental)
  • Meningitis/encephalitis
  • Schizophrenia
  • Sepsis
  • SSRI toxicity

Complications

  • Hypoglycemia
  • Seizures
  • Myocardial infarction
  • Rhabdomyolysis
  • Coma
  • Intraparenchymal hemorrhage
  • Subarachnoid hemorrhage

Enhancing Healthcare Team Outcomes

PCP toxicity is best managed by a multidisciplinary team that also includes ER and ICU nurses. The majority of patients require supportive treatment with close monitoring of hemodynamics. In mild cases, recovery is possible within6-12 hours. Severe cases may require admission to the ICU. Prior to discharge, a mental health nurse consult may be required to determine if this was accidental or an intentional overdose.


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Phencyclidine (PCP) Toxicity - Questions

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A patient presents with psychotic behavior after ingestion of an illicit drug. Examination reveals hypertension and nystagmus. What is the best medication to protect against seizures in this patient?



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A patient presents with psychotic behavior after ingesting an illicit drug. Examination reveals hypertension and rotary nystagmus. To protect against seizures, what medication should be used?



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A patient is brought to the emergency department by the police with suspected phencyclidine toxicity. He exhibits agitation and psychosis. Which of the following would be least important in the management of this patient?



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A young man is brought to the emergency room because of behavior problems. His friend says that he has a history of using illicit drugs. The individual appears to be hallucinating, euphoric, and extremely agitated. He has reddish skin, slurred speech, and a very unsteady gait. An ocular exam reveals dilated pupils with nystagmus. Which of the following drugs was most likely ingested?



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Which of the following symptoms and signs is NOT caused by phencyclidine overdose?



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What is the most common therapeutic intervention for an individual who has used phencyclidine (PCP)?



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Which of the following illicit drugs is mostly associated with hallucination and aggression?



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A 15-year-old is transported to the emergency department by paramedics. He is confused and disoriented. There is muscle rigidity, increased deep tendon reflexes, increased salivation, and nystagmus. He is hypertensive and catatonic. Which of the following is the most likely diagnosis?



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Select the recreational drug that causes dissociative anesthesia.



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Which of the following substances can cause labile affect, vertical nystagmus, increased pain tolerance, muscle rigidity, ataxia, and dysarthria?



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A patient presents to the emergency department with acute phencyclidine toxicity. Which of the following is false?



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A 17-year-old male presents the emergency department via emergency medical services for altered mental status after intravenous use of phencyclidine. The patient is extremely agitated requiring physical restraint. He has a heart rate of 145 bpm, blood pressure 170/90 mmHg, respiratory rate of 22/minute, and oxygen saturation of 90% on room air. Fingerstick blood glucose is 102 mg/dL. He is warm to the touch, diaphoretic and has rotary nystagmus. The patient then begins to have a generalized seizure. The patient has no IV access. What is the next most appropriate step?



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A 17-year-old male brought to the emergency department by law-enforcement for “bizarre behavior.” The patient is extremely agitated and uncooperative requiring physical restraint by four police officers. The patient has a heart rate of 135 bpm, blood pressure 177/82 mm of Hg, respiratory rate 26 breaths/minute, oxygen saturation 92% on room air. Fingerstick blood sugar 110 mg/dL. The patient is given 4 mg IM lorazepam for sedation. The patient is warm to the touch. Eye exam shows miotic pupils and rotary nystagmus. Police state that witnesses report that the patient was smoking “angel dust” before exhibiting his “bizarre behavior.” Which of the following is false pertaining to the substance that the patient has been using?



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Which of the following is not a potential complication of phencyclidine (PCP) intoxication?



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Phencyclidine (PCP) Toxicity - References

References

Wallach J,Brandt SD, 1,2-Diarylethylamine- and Ketamine-Based New Psychoactive Substances. Handbook of experimental pharmacology. 2018 Sep 9;     [PubMed]
Grayson B,Barnes SA,Markou A,Piercy C,Podda G,Neill JC, Postnatal Phencyclidine (PCP) as a Neurodevelopmental Animal Model of Schizophrenia Pathophysiology and Symptomatology: A Review. Current topics in behavioral neurosciences. 2016;     [PubMed]
Misselbrook GP,Hamilton EJ, Out with the old, in with the new? Case reports of the clinical features and acute management of two novel designer drugs. Acute medicine. 2012;     [PubMed]
Meltzer HY,Horiguchi M,Massey BW, The role of serotonin in the NMDA receptor antagonist models of psychosis and cognitive impairment. Psychopharmacology. 2011 Feb;     [PubMed]
Koseki T,Nabeshima T, [Phencyclidine abuse, dependence, intoxication, and psychosis]. Nihon rinsho. Japanese journal of clinical medicine. 2010 Aug;     [PubMed]
Schwartz RH, Adolescent abuse of dextromethorphan. Clinical pediatrics. 2005 Sep;     [PubMed]
Morris BJ,Cochran SM,Pratt JA, PCP: from pharmacology to modelling schizophrenia. Current opinion in pharmacology. 2005 Feb;     [PubMed]

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